TY - JOUR
A2 - Fonseca-Camarillo, Gabriela
AU - Xu, Hao-ming
AU - Zhou, You-lian
AU - Xu, Jing
AU - Li, Ying-fei
AU - Zhao, Chong
AU - Huang, Hong-li
AU - Du, Yan-lei
AU - He, Jie
AU - Zhou, Yong-jian
AU - Nie, Yu-qiang
PY - 2021
DA - 2021/01/08
TI - Inhibition of PD-1 Protects against TNBS-Induced Colitis via Alteration of Enteric Microbiota
SP - 4192451
VL - 2021
AB - Background and Aim. The enteric microbiota is able to cross-talk with factors involved in the blockade of programmed cell death protein 1 (PD-1) and also plays an important role in the predisposition and onset of inflammatory bowel disease (IBD). The current study used a mouse model of experimental colitis to determine the pathogenic connection between PD-1 inhibition, gut microbiota, and IBD. Methods. Colitis was induced in mice using 2,4,6-trinitrobenzene-sulfonic acid (TNBS), and mice were subsequently treated with either a PD-1 inhibitor or 5-amino-salicylic acid (ASA) as a positive control. Body weight, disease activity index (DAI), colon length, and tissue damage were evaluated, and the enteric microbiota was profiled using high-throughput 16S rRNA sequencing of fecal samples from the experimental mice. Results. TNBS caused mice to experience IBD-like symptoms, which were attenuated by the PD-1 inhibitor, as indicated by a decrease in DAI scores (p=0.0002). Furthermore, in this mouse model of IBD, PD-1 inhibition improved the alpha diversity as well as restored the beta diversity of the enteric microbiome. It also significantly enriched the abundance of short-chain fatty acid- (SCFA-) producing bacteria of the Firmicutes (p<0.05) and Bacteroidetes (p<0.05) phyla but depopulated Proteobacteria (p<0.05). Conclusion. PD-1 inhibition can partly mitigate TNBS-induced colitis and restore the enteric microbiota by enriching the abundance of SCFA-producing bacteria.
SN - 2314-6133
UR - https://doi.org/10.1155/2021/4192451
DO - 10.1155/2021/4192451
JF - BioMed Research International
PB - Hindawi
KW -
ER -